P2X2, control peptide, 100 ug.
- Known as:
- P2X2, reference short protein sequence, 100 ug.
- Catalog number:
- P10109
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- P2X2 control peptide 100 .
Related genes to: P2X2, control peptide, 100 ug.
- Gene:
- P2RX2 NIH gene
- Name:
- purinergic receptor P2X 2
- Previous symbol:
- DFNA41
- Synonyms:
- P2X2
- Chromosome:
- 12q24.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-30
- Date modifiied:
- 2016-02-05
Related products to: P2X2, control peptide, 100 ug.
Related articles to: P2X2, control peptide, 100 ug.
- Activating mutations in the epidermal growth factor receptor () gene drive non-small cell lung cancer (NSCLC). Oncogenic EGFR mutants are ligand-independent and more stable, but the underlying mechanism remains unclear. We hypothesized that EGFR mutants selectively leverage cellular stabilizers to evade degradation. Genome-wide RNA interference screens identified genes (encoding for stabilizers) responsible for mutant EGFR stability, with P2Y2 receptor (P2Y2) emerging as a bona fide stabilizer. Mechanistically, high extracellular adenosine triphosphate (ATP) levels transactivate EGFR mutants via P2Y2 activation, previously shown to signal through Src kinase-dependent EGFR phosphorylation. Our study reveals that ATP-driven P2Y2 activation stabilizes EGFR mutants by forming a P2Y2-integrin β1-EGFR complex enriched in endosomes. Targeting this axis destabilizes EGFR mutants and offers a strategy against drug resistance. Elevated P2Y2 and integrin β1 expression in patients with NSCLC implies clinical relevance. Our results provide previously unidentified insight that EGFR mutants enhance extracellular ATP levels to activate P2Y2-integrin for enhanced stability of EGFR mutants to drive the oncogenic program. - Source: PubMed
Publication date: 2026/01/21
Du YafeiWang WenjingGoh Hui ChinVaiyapuri Thamil SelvanRaju AnandhkumarHsiao Yu-ChunWang Cheng ChunAgrawal VanishaMohideen Noorul FarzanaMohd Mazian Norhidayah BinteKaratekin FerideWang Wendy KehanLakshmanan ManikandanGupta KomalChang HanLe Guezennec XavierBard FredericTan Daniel S WTergaonkar VinayHung Mien-ChieLiu XiaogangHong WanjinBoopathy Gandhi T K - Gastric cancer (GC) prevention and treatment have always been a difficult problem to solve. Therefore, mining the molecular genes related to the progression of GC and predicting the progression of GC has important clinical significance. Therefore, this study investigated whether the P2Y2 receptor (P2Y2R) has a certain effect on GC. - Source: PubMed
Publication date: 2025/12/16
Wu Yu-QingWang Wen-Long - While the etiology of Meniere's disease (MD) is likely multifactorial, genetics are thought to play a role. Several previous studies have yielded inconclusive results, potentially due to phenotypic uncertainty and variable diagnostic criteria. To explore potential genetic bases in a more rigorous context, we assessed the clinical predictors and diagnostic yield of current hearing loss panels in a highly curated cohort of patients with bilateral and/or early-onset MD. - Source: PubMed
Publication date: 2025/12/09
Shah Keshav VJung ChristianTalian DanielDavis SherrieEpstein Douglas JRuckenstein Michael JHwa Tiffany P - Genome editing has the potential to treat genetic hearing loss. However, current editing therapies for genetic hearing loss have shown efficacy only in hearing rescue. In this study, we evaluated a rescue strategy using adeno-associated virus (AAV) type 2-mediated delivery of Staphylococcus aureus Cas9-sgRNA in the mature inner ear of the P2rx2V61L/+ mouse model of autosomal dominant deafness-41 (DFNA41), a dominant, delayed-onset, and progressive hearing loss in humans. We demonstrate that local injection in adult mice results in efficient and specific editing that abolishes the mutation without notable off-target effects or AAV genome integration. Editing effectively restores long-term auditory and vestibular function. Editing further protects P2rx2V61L/+ mice from hypersensitivity to noise-induced hearing loss, a phenotype also observed in patients with DFNA41. Intervention in mice at a juvenile stage broadens the frequency range rescued, highlighting the importance of early intervention. An effective and specific gRNA for the human P2RX2 V60L mutation has been identified. Our study establishes the feasibility of editing to treat DFNA41 caused by P2RX2 V60L mutation in humans and opens an avenue for using editing to rescue hearing and vestibular function while mitigating noise-induced hearing loss. - Source: PubMed
Publication date: 2025/08/14
Wei WeiZhu WenliangSilver StewartArmstrong Ariel MRobbins Fletcher SRameshbabu Arun PrabhuWalz KatherinaQuan YizhouDu WanKim YehreeIndzhykulian Artur AShu YilaiLiu Xue-ZhongChen Zheng-Yi - Hearing loss is genetically heterogeneous, with over 121 implicated genes. Minor allele frequency (MAF) data from population databases greatly aid variant interpretation; however, these databases are predominantly based on individuals of European ancestry and lack sufficient East Asian representation, limiting accurate interpretation in under-represented populations. We analyzed rare variants associated with non-syndromic hearing loss classified as pathogenic, likely pathogenic, or of uncertain significance in the Deafness Variation Database (DVD). Population allele frequencies from 9,579 Koreans, 54,000 Japanese, and 651 patients with sensorineural hearing loss were evaluated. Of the 6,381 pathogenic or likely pathogenic variants cataloged in the DVD, 216 (3.38%) were detected in Korean population. Among these, 31 variants exhibited high allele frequencies that exceeded thresholds typically applied to identify benign variants in clinical interpretation guidelines. Of these, 6 remained disease-causing, including 4 East Asian founder alleles and one MYO7A variant common in Koreans. Our pipeline identified 24 variants for reclassification as benign or likely benign, and one P2RX2 variant of uncertain significance. Of 1,299,211 VUS, 3,736 were reclassified as benign. A substantial number of variants previously classified as pathogenic were reclassified as benign using MAF data from under-represented populations, highlighting the need for large-scale sequencing in diverse ancestries. - Source: PubMed
Publication date: 2025/09/29
Joo Sun YoungJang Seung HyunKim Jung AhKim Se JinChoi Jae YoungJung JinseiGee Heon Yung